Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Erik's IHO Week 6 > 5-31 KRAFTS Thrombotic Disorders > Flashcards

5-31 KRAFTS Thrombotic Disorders Flashcards

1
Q

What happens when and embolus breaks off a DVT?

A

Goes through veins, back to heart, into lungs and causes pulmonary
embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are symptoms of DVT (deep venous thrombosus)?

A

Hot, red leg (b/c blood can get in but not out)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is Virchow’s Triad?

A

Factors contributing to thrombosis
Endothelial Damage
Stasis
Hypercoagubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is “stasis?”

A

Not moving (like sitting on a plane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why does stasis contribute to thrombosis?

A

Blood pools and platelets and clotting factors can come together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What molecule can carcinoma cells release which increase risk of clotting?

A

Mucin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What factors would make you think a patient might have a Hereditary Thrombotic Disorder?

A 
Young patient
	No obvious cause
	Family history
	Recurrent episodes
	Weird location (anywhere other than leg)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 4 things you must know about FACTOR V LEIDEN?

A

Most common cause of unexplained thromboses
Point mutation in Factor V gene
Factor V can’t be turned off
Dx: genetic testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why can’t Factor V be turned off in Factor V Leiden?

A

The genetic mutation prevents its cleavage by Protein C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Are PTT and INR helpful in Factor V Leiden Dx?

A

NO. Patient clots just fine, so those tests won’t show anything.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do you treat Factor V Leiden?

A

Don’t, unless there’s a Thrombosis
Then: give anticoagulant (usually Coumadin)
If recurrent episodes, consider long term anticoagulant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 4 things you must know about ANTITHROMBIN III DEFICIENCY?

A

ATIII is natural anticoagulant
ATIII potentiated by Heparin
Many gene mutations exist
Very rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does ATIII inhibit?

A

Factors IIa (thrombin), VIIa, IXa, Xa, and Xia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Can you do genetic testing for ATIII deficiency?

A

No – too many possible mutations to test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How to you test for ATIII deficiency?

A

Functional testing: take patient’s plasma, put thrombin in it, later see how much thrombin is still active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Can homozygotes for ATIII def live?

A

Nope

17
Q

Tx of ATIII def?

A

ATIII concentrates required

18
Q

What are the 2 things you must know about PROTEIN C and S DEFICIENCIES?

A

Warfarin-induced skin necrosis

C deficiency rare; S deficiency super-rare

19
Q

What factors does Protein C inhibit?

A

Factor Va and VIIIa

20
Q

What is protein S?

A

Endothelial cell receptor for protein C

21
Q

Dx of Protein C/S def?

A

Functional testing

22
Q

What’s causing the deficiency of Protein C/S?

A

Genetic mutation – many different kinds

23
Q

What inhibits Proteins C and S?

A

Warfarin!

24
Q

How does Warfarin induce skin necrosis in protein C and S deficiencies?

A

Warfarin -> ↓Protein C and S -> Hypercoagulation -> clots -> necrosis

25
Q

What is purpura fulminans?

A

Thrombotic state + vascular injury = skin necrosis

Related to Warfarin-induced skin necrosis

26
Q

What is Purpura Fulminans associated with?

A

Coagulopathies

Sepsis (huge mortality rate)

27
Q

Tx of Purpura Fulminans?

A

Give protein C

28
Q

What are the 4 things you must know about FACTOR II GENE MUTATION?

A

Factor II = prothrombin
Mutated gene  ↑prothrombin
Prothrombin itself is normal
Rare in non-Caucasians

29
Q

What are the 4 things you must know about HYPERHOMOCYSTEINEMIA?

A

Homocysteine converts folate
Homocysteinuria = rare metabolic disorder
Too much homocysteine = thromboses
Homocysteinemia has many causes

30
Q

What is bad about too much homocysteine?

A

Toxic to endothelium (via ROS)

Interferes w/ NO (vasodilator and antithrombotic)

31
Q

What are the 4 things you must know about ANTIPHOSPHOLIPID ANTIBODIES?

A

Auto-Ab’s against phospholipids
Falsely ↑INR
May cause thromboses
Antiphospholipid syndrome is serious

32
Q

What kind of Ab’s are antiphospholipid Ab’s?

A

IgG

33
Q

What do the Antiphospholipid Ab’s do?

A

Bind to phospholipids

Screw up tests

34
Q

What’s an easier name for Antiphospholipid Ab’s?

A

Inhibitors (inhibit coagulation in vitro)

35
Q

What is the paradox surrounding these inhibitors?

A

Inhibit coag in vitro

BUT they promote coag in vivo!

36
Q

How do you detect these Ab’s?

A

PTT Mixing study! If PTT doesn’t correct, inhibitors are present

37
Q

What is Antiphospholipid Antibody Syndrome?

A 
Recurrent thrombosis
	Recurrent spontaneous abortions
	Increased stroke risk
	Pulmonary hypertension (clots in lungs)
	Renal failure (clots in kidneys)
38
Q

Under what conditions might you see these Ab’s develop?

A

Kids – infection
Adults – autoimmune disease
Elderly - drugs

Erik's IHO Week 6 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions